Snapshots from Durban
Many of the scientific and treatment issues covered at Durban, and in the following pages, are presently clinically irrelevant to most HIV-positive women worldwide. Heightened levels of women's advocacy and research have begun to close this gap. But, a great deal of work still needs to be done to make research more meaningful to all women. This requires economic and social change, as well as a real commitment by researchers, politicians, industry, advocates and people living with HIV alike.
Human papilloma virus (HPV), the sexually transmitted virus that causes genital warts, is linked to developing cervical and anal pre-cancerous conditions (called dysplasia) and cancer. Studies show that compared to HIV-negative women, women with HIV -- particularly those with low CD4+ cell counts -- have a higher rate and severity of HPV-related cervical dysplasia. Several studies presented at Durban confirmed these findings, underscoring the need for regular GYN exams to screen for HPV-related dysplasia in order to detect and treat early signs of cervical cancer.
Like cervical HPV, anal HPV and dysplasia is common in HIV-positive women. In fact, in one recent study, anal HPV proved to be more common than cervical HPV in HIV-positive women and their negative counterparts. Among HIV-positive women, other risk factors for anal HPV included lower CD4+ cell count, presence of cervical HPV, younger age and Caucasian/white race.
Because anal HPV is linked to increased risk of anal dysplasia -- a precursor to anal cancer -- these results may indicate an increased risk of developing anal cancer. Moreover, they suggest the importance of regular anal exams to detect anal dysplasia. This procedure is not currently or routinely performed in women or men. Like cervical Pap smears, some researchers and health advocates argue that including anal Pap smears in routine healthcare visits could catch dysplasia early and prevent progression to cancer.
There were numerous presentations on lipodystrophy (the general term describing fat redistribution and lab value changes, like cholesterol). The overall picture of what lipodystrophy is, what it's caused by and how and if it can be treated remains unclear. What is clear is that lipodystrophy is a real concern for many people living with HIV. One study found that it's an increasingly common reason why some people decide to stop, delay or switch therapy.
Several studies tried to determine risk factors for lipodystrophy. Some found a connection between d4T (stavudine, Zerit) use and fat loss, and between protease inhibitor use -- especially ritonavir (Norvir) and indinavir (Crixivan) -- and fat gain. Older age and sex may be important factors, too. Several studies showed that women may experience more fat gain, and men more fat loss. Other factors include advanced HIV disease, duration of disease and duration of earlier anti-HIV therapy. Unfortunately, many of these studies continue to use different definitions and ways to measure it, making it difficult to compare one to another and draw conclusions. The field remains full of contradictions and unexplained phenomena.
Many women living with HIV also live with hepatitis C virus (HCV). The effect of living with both viruses (called co-infection) on pregnancy and mother-to-child transmission is a new area of research. Some studies suggest that co-infection is connected to increased risk of HCV transmission. However, more research is needed to determine if this really is the case.
A study of 509 co-infected women con-ducted in Europe looked at the effects of mode of delivery and infant feeding on risk of HCV transmission. Women who delivered by C-section were much less likely to transmit HCV than women who delivered vaginally. While only 13 women breast-fed, breast-feeding was significantly associated with HCV transmission compared to other forms of feeding (35% vs. 13%). Similarly, children who were HIV-positive were also more likely to be HCV-positive than children who were not infected with HIV.
These findings suggest a possible interaction between HIV and HCV that may affect the risk of mother-to-child transmission. More research to determine the nature of this interaction and possible risks of co-infection on disease progression in both mother and child is needed.
Preventing mother-to-child HIV transmission was one of the major themes of the conference. Results from several studies suggest that very short courses of therapy with either nevirapine (Viramune), or AZT (Retrovir, zidovudine), or AZT and 3TC (Epivir, lamivudine, the combination of AZT+3TC is Combivir), are able to lower transmission rates by about 50%. With better access to therapy, it's possible to significantly reduce vertical transmission rates in resource poor countries.
The Achilles heel of preventing mother-to-child HIV transmission remains breast-feeding -- a necessity for many women around the world. Two major studies report a decrease in the protective effect of short-course anti-HIV therapy to reduce transmission as a result of breast-feeding.
By 12 to 18 months after birth, transmission rates rose to 24% and then 30%, respectively, as babies became infected through breast-feeding. Thus, strategies to reduce mother-to-child HIV transmission must address related social and economic issues, such as child feeding.
There are several studies now looking at different kinds of strategies for safer breast-feeding. Early results from one such study suggest that mixed breast-feeding -- where breast milk is supplemented with cereal, juice, water and so forth -- has a higher risk of transmission than exclusivebreast-feeding. Interestingly, there was no difference between the rates of transmission among women who exclusively breast-fed or exclusively formula-fed their children. More study is needed to determine the reason for these surprising results.
There's a growing trend of people stopping or switching their anti-HIV regimens. Reasons for stopping or downshifting (changing from a HAART to a non-HAART regimen) are often related to side effects, treatment fatigue, stage of HIV disease or lifestyle issues.
One large study of over 1,000 women reported that, after three years on HAART, 20% of them switched to less intensive regimens. Another 17% stopped therapy altogether. Women with low viral load and high CD4+ cell counts were just as likely to stop or downshift therapy as women with high viral load and low CD4+ cell counts. This suggests that the response to treatment is not necessarily the reason people decide to stop or switch therapies. More research is needed to understand the effects of reducing or stopping therapy in this group of women.
Whatever the reasons you may have for switching or stopping therapy, it is always good to talk them over with a doctor before actually switching or stopping the drug(s).
This article was provided by Project Inform. It is a part of the publication WISE Words. Visit Project Inform's website to find out more about their activities, publications and services.